Encephalitis is a rare complication of rubella virus infection. Its pathophysiology is not well established. [1]

A 27-year-old patient was admitted for generalized tonic-clonic seizure and altered mental status. Four days before admission, he had had fever and a maculopapular rash on the torso for which he had been treated with cefuroxime; however, his neurologic state had progressively deteriorated. He had no history of vaccination against rubella. On examination, he was febrile (39°C) and had a maculopapular skin rash over the face and torso. Neurological examination revealed a comatose patient with a Glasgow Coma Scale (CCS) score of 5, bilateral brisk tendon reflexes, bilateral extensor plantar response, and signs of meningeal irritation. The pupils were equal, round, and reactive to light; the brainstem reflexes were normal. Cranial computed tomography (CT) scan showed no abnormality. Cerebrospinal fluid (CSF) analysis showed glucose 5.8 mmol/l (corresponding serum glucose: 11.4 mmol/l), protein 2.08 g/l, and cell count 270 mm 3 (all lymphocytes). Magnetic resonance imaging (MRI) done 24 h later was normal. An enzyme-linked immunosorbent assay (ELISA) was positive for rubella IgM antibodies in the CSF (a titer of

38 UI/ml) and in the serum [a titer of 120 UI/ml (normal range below 1.2)]. Bacterial cultures were negative, and antibodies against herpes simplex virus were also negative. The patient was sedated, intubated, and mechanically ventilated as he was in deep coma and had aspiration. He showed improvement in his clinical status, becoming fully conscious within 2 days. He was weaned off mechanical ventilation within 3 days and was discharged from ICU 5 days later.

Rubella is a mild viral illness that usually occurs in children between 5 and 14 years of age, but it can also occur in adults, when it may follow a more severe clinical course. [1] Neurologic complications are rare, with the reported incidence varying from 1 in 6000 to 1 in 24000. [2] Encephalitis most often occurs within 1-6 days of the development of the typical rash; however, cases of encephalitis without a rash have also been reported. [1] The exact mechanism of rubella encephalitis is not well established and two hypotheses have been proposed: Direct viral invasion and an immune-mediated response. [3] Rubella virus has been known pantropic to nerve cells and has the ability to spread through the nervous system. [3] Autopsy studies in patients with rubella encephalitis have revealed diffuse nonspecific neural degeneration, edema, and perivascular lymphocyte infiltrate without demyelination and pronounced inflammatory damage. [4]

In Tunisia, rubella encephalitis has not been previously reported and vaccination against rubella virus has only recently been included in the national vaccination program. In our patient, the diagnosis was confirmed by the presence of rubella IgM antibodies in the CSF and the serum. Unlike in sub-Saharan African countries, other causes of fever with altered sensorium, e.g., malaria or typhoid, are rare in Tunisia. The severity of encephalitis as a complication of rubella infection is widely variable and an overall mortality rate of 20% has been reported. [5] This emphasizes the importance of vaccination in preventing severe life-threatening complications such as encephalitis. Phylogenic studies should be performed in order to identify a possible viral mutation that could explain this unusual complication of rubella infection.